Cellular distribution of IDH mutations in AML during morphologic remission.

Limited information exists about the cellular distribution of mutations which persist in remission in acute myeloid leukemia (AML) (variably considered pre-leukemic mutations). We hypothesized that mutations detectable in all cell compartments may be less pathogenic than those that are myeloid-restricted. Here, we describe the cellular compartments that have IDH mutations in five patients with IDH-mutated AML in morphologic remission. Unlike pre-leukemic clones harboring the more common DNMT3A, TET2 and ASXL1 (DTA) mutations, we show that IDH mutations are myeloid-restricted. This finding provides an explanation for the reports that IDH mutations carry a higher risk for relapse than DTA mutations. Detailed analysis of one case also shows acquisition of additional mutations in distinct cellular compartments, illustrating subclonal complexity associated with therapeutics.

Acute respiratory distress syndrome precipitated by granulocyte colony-stimulating factor in undiagnosed Pneumocystis jirovecii pneumonia.

We present the case of a 62-year-old man with rheumatoid arthritis who developed a leukaemoid reaction and acute respiratory distress syndrome (ARDS) following granulocyte colony-stimulating factor (G-CSF) administration that had been given to treat neutropenia secondary to methotrexate and leflunomide toxicity. Later it was established that he had Pneumocystis jirovecii pneumonia, which was treated to complete resolution with a course of corticosteroids and antibiotics. This case highlights the potential risk of G-CSF administration in an immune compromised individual in the midst of bone marrow recovery in the context of active infection. Recognition of immune escape syndromes is vital and requires an understanding of potential triggers and risk factors.

In Vivo Laser Confocal Microscopy Using the HRT-Rostock Cornea Module: Diversity and Diagnostic Implications in Patients with Uveitis.

PURPOSE: Keratic precipitates (KP) are a common feature of uveitis. We prospectively examined KP with the Heidelberg Retinal Tomograph II confocal laser scanning microscope and Rostock Corneal Module (HRT-RCM) to explore their diagnostic implications. METHODS: Prospective, observational, multicenter study. HRT-RCM images were classified by two masked observers. RESULTS: 120 scans on 120 eyes from 110 subjects were included. The majority (N = 93) had non-infectious uveitis. Sixty eyes had active disease at scanning. Eight KP morphologies were defined. Agreement between the two masked graders was high (Kappa value across all categories = 0.81). Cluster and nodular KP were associated with active infectious uveitis (p < 0.01): patients with cluster KP (odds ratio [OR] = 3.03, 95% confidence interval [CI]: 1.43, 6.45) and nodular KP (OR = 3.89, 95% CI: 1.42, 10.65) were more likely to have infectious uveitis than those without. CONCLUSIONS: Laser confocal microscopy of KP may have a role in determining between infectious and non-infectious uveitis.